Mucosal necrosis
Necrosis is a disease that leads to the death of cells and tissues. Often the surface of the oral mucosa, digestive tract and other organs is affected by necrosis due to locally acting irritants - mechanical, chemical, bacterial. Also, the destruction of the mucous membrane is caused by any disorders of the body, for example, vitamin deficiency, infectious diseases, blood diseases, metabolic disorders, etc.
Violation of the trophism of the oral mucosa is facilitated by vascular diseases, severe forms of diabetes mellitus and complications after urological and abdominal operations. With chemical burns of the oral mucosa with acids, arsenous paste, phenol, formalin, nitrate, etc., coagulation necrosis occurs. Alkalis cause colliquation necrosis. The defeat covers all layers of soft tissues, on the gums and hard palate.
With proper treatment, after a few days, the necrotic tissue is rejected and the erosions or ulcers slowly heal. The mechanism of development of necrosis of the oral mucosa is triggered in diseases of the blood and hematopoietic organs. Changes in the mucous membrane in some cases appear earlier than the clinical signs of the underlying disease. Ulceration of the mucous membrane with subsequent necrosis is often observed in acute leukemia. Bleeding, looseness of the gums, cheeks, tongue, necrosis of the apex of the gum papilla are noted, it becomes cyanotic.
The entire mucous membrane becomes pale, anemic. Necrosis develops at a rapid pace, an ulcer forms around the tooth with a dark gray coating with a fetid odor. Reveal necrosis on the tonsils and other parts of the oral cavity. As a result of the necrotic process in acute leukemia, foci are formed, with very extensive ulcers of irregular contours, which are covered with a gray necrotic plaque.
Oral necrosis is manifested by severe pain during meals. Patients complain of difficulty in swallowing, putrid fetid odor from the mouth. There is also general weakness, dizziness, headache, a decrease in the amount of saliva secreted due to dystrophic processes in the salivary glands. The development of necrosis is due to the action of external factors, mainly microorganisms.
The onset of the pathology is characterized by a deterioration in the general condition of the patient. The temperature may rise, a dirty gray plaque appears in the oral cavity, edema and hyperemia of the mucous membrane of the soft palate, anterior palatine arches and pharynx. After a while, there is a slightly edematous, loose white, practically unremovable plaque, similar to thrush. Then there is a change in color to gray-green, confirming the presence of necrotic processes that progress at a high speed.
The bone tissue of the jaw and lips are affected, necrosis spreads to the digestive tract, lymph nodes increase, and the number of leukocytes decreases. Elimination of traumatic factors and prophylactic oxygen therapy of the oral cavity, reduction of the effect of tissue trophism disorders, elimination of the action of pathogenic microflora can reduce the activity of ulcerative-necrotic processes in the oral cavity.
An improvement in the condition of the mucous membrane is characteristic of the use of antiseptic solutions, painkillers and drugs that accelerate epithelization. The complex of therapeutic measures includes a gentle diet, the use of vitamins.
The reasons that can lead to acute necrosis of the esophageal mucosa include arterial hypertension, ischemia, hyperglycemia, allergy to antibiotics, infectious lesions, intestinal obstruction, aortic rupture. Alkali burn, melanosis, malignant melanomas and acanthosis nigricans are accompanied by acute necrosis of mucous surfaces. The maximum changes in the esophageal mucosa are determined in the distal part.
Necrosis of the mucous membrane (black esophagus) is expressed in inflammation and partial destruction of muscle fibers. Thrombosis of the blood vessels is observed, but due to the development of a scab on the walls of the esophagus, the spread of necrosis to the deep layers of the membrane is prevented. The positive dynamics of the treatment provides the formation of a thick white plaque, which can be cleaned to reveal pink granulation tissue.
Usually, the disease provokes gastrointestinal bleeding, the development of severe complications, for example, esophageal stenosis and the formation of strictures.
Therapeutic methods of treatment should be aimed primarily at preventing sepsis, improving microcirculation, and arresting the gastroesophageal reflex. It is imperative to introduce proton pump inhibitors, to normalize the motility of the gastrointestinal tract.
Article author: Mochalov Pavel Alexandrovich | d. m. n. therapist
Education: Moscow Medical Institute. IM Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational Diseases", in 1996 "Therapy".
